In one paragraphArticle in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registryThe trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
19 authors.
Philip R TedburyCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0000-0001-8151-4967 Darius MahboubiCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0000-0001-9279-997X Maritza Puray-ChavezDepartment of Molecular Microbiology & Immunology, University of Missouri School of Medicine; Columbia, MO, USA.ORCID 0000-0002-7983-0757 Raven ShahCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.
Obiaara B UkahDepartment of Molecular Microbiology & Immunology, University of Missouri School of Medicine; Columbia, MO, USA.
Claudia C WahoskiCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.
Hind J FadelDivision of Infectious Diseases, Anschutz Medical Campus, University of Colorado School of Medicine; Aurora, CO, USA.
Eric M PoeschlaDivision of Infectious Diseases, Anschutz Medical Campus, University of Colorado School of Medicine; Aurora, CO, USA.
Xinlin GaoCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0009-0002-2518-235X William M McFaddenCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0000-0001-6911-2172 Maria GaitanidouCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0009-0000-0489-6295 Nikolaos KesesidisCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0000-0002-3179-1066 Karen A KirbyCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0000-0003-2468-4796 Thomas H VanderfordDivision of Microbiology and Immunology, Emory National Primate Research Center, Emory Vaccine Center, Emory University; Atlanta, GA, USA.
Mamuka KvaratskheliaDivision of Infectious Diseases, Anschutz Medical Campus, University of Colorado School of Medicine; Aurora, CO, USA.ORCID 0000-0003-3800-0033 Vasudevan AchuthanDepartment of Cancer Immunology and AIDS, Dana-Farber Cancer Institute; Boston, MA, USA.
Ryan T BehrensDepartment of Pathology and Laboratory Medicine, University of Wisconsin-Madison; Madison, WI, USA.
Alan N EngelmanDepartment of Cancer Immunology and AIDS, Dana-Farber Cancer Institute; Boston, MA, USA.ORCID 0000-0002-9709-2591 Stefan G SarafianosCenter for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.ORCID 0000-0002-5840-154X Funding
Virology and Molecular Biomarkers CoreP30AI050409 · NIAID · EMORY UNIVERSITY · PI Ann M Chahroudi, Colleen F Kelley · 2002 to 2026
$74.0MStructural Biology CoreU54AI170855 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI Stefan G Sarafianos, Bruce Edward Torbett · 2022 to 2026
$36.7MNovel mechanism of integrase (IN) resistance to Dolutegravir through epistatic interactions between IN and the nucleocapsid and polypurine tract regions of HIV-1R01AI146017 · NIAID · EMORY UNIVERSITY · PI HACHIYA, ATSUKO, LYUMKIS, DMITRY · 2019 to 2023
$2.6MRole of HIV-1 integrase in virion morphogenesis and its targeting by allosteric integrase inhibitorsR01AI184419 · NIAID · UNIVERSITY OF COLORADO DENVER · PI JAMES R FUCHS, Sebla B. Kutluay · 2024 to 2026
$2.4MStructural and Biochemical Effects of Capsid-targeting Molecules on HIV-1 Capsid AssemblyF31AI174951 · NIAID · EMORY UNIVERSITY · PI WILLIAM MICHAEL MCFADDEN · 2023 to 2026
$196kNIAID NIH HHS F31 AI174951NIAID NIH HHS P30 AI050409NIAID NIH HHS R01 AI146017NIAID NIH HHS R01 AI184419NIAID NIH HHS U54 AI170855
6 · The paper itselfAbstract
Disruption of HIV-1 Integrase (IN) interactions with the host-factor Lens Epithelium-Derived Growth Factor (LEDGF)/p75 leads to decreased, random integration, increased latent infection, and described here, accumulation of HIV-1 antisense RNA (asRNA). asRNA increase was observed following interruptions of IN-LEDGF/p75 interactions either through pharmacologic perturbations of IN-LEDGF/p75 by treatment with allosteric HIV-1 integrase inhibitors (ALLINIs) or in cell lines with LEDGF genetic knockout. Additionally, by impairing Tat-dependent HIV transcription, asRNA abundance markedly increases. Illumina sequencing characterization of asRNA transcripts in primary T cells infected in the presence of ALLINIs showed that most initiate from within the HIV-1. Overall, loss of IN-LEDGF/p75 interactions increase asRNA abundance. Understanding the relationship between ALLINIs, integration sites, asRNA, and latency could aid in future therapeutic strategies.
Identifiers
PMID39677798
PMCPMC11643104
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